Iron deposits in the chronically inflamed central nervous system and contributes to neurodegeneration.
Iron deposits in the chronically inflamed central nervous system and contributes to neurodegeneration.
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DOI：
10.1007/s00018-013-1509-8
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发表时间：
2014-05
影响因子：
8
通讯作者：
Moos, Torben
中科院分区：
文献类型：
--
作者：
Andersen, Hjalte Holm;Johnsen, Kasper Bendix;Moos, Torben
关键词：
神经退行性疾病的特征在于在具有神经元细胞死亡的区域中存在炎症，并且铁的区域性增加超过正常老化期间发生的情况。伴随神经元变性的炎性过程涉及中枢神经系统（CNS）的神经胶质细胞和迁移到CNS中同时转化为吞噬巨噬细胞的循环的单核细胞。本文综述了神经退行性疾病中铁沉积的可能机制，主要强调含铁单核细胞如何迁移到中枢神经系统，转化为巨噬细胞，并在吞噬受损和垂死的神经细胞后死亡。垂死的巨噬细胞可能反过来释放它们的铁，铁进入不稳定的铁池，以催化促进自由基介导的应激和对相邻细胞（包括神经元）的氧化损伤的形成。健康的神经元也可以长期从细胞外空间获得铁，作为氧化应激介导的损伤的另一个主要机制。单核细胞迁移到中枢神经系统的药理学处理结合螯合剂，中和细胞外铁的影响，由于从垂死的巨噬细胞释放以及神经元内螯合可能表示减少铁沉积在中枢神经系统中的有害后果的良好可能性。
Neurodegenerative disorders are characterized by the presence of inflammation in areas with neuronal cell death and a regional increase in iron that exceeds what occurs during normal aging. The inflammatory process accompanying the neuronal degeneration involves glial cells of the central nervous system (CNS) and monocytes of the circulation that migrate into the CNS while transforming into phagocytic macrophages. This review outlines the possible mechanisms responsible for deposition of iron in neurodegenerative disorders with a main emphasis on how iron-containing monocytes may migrate into the CNS, transform into macrophages, and die out subsequently to their phagocytosis of damaged and dying neuronal cells. The dying macrophages may in turn release their iron, which enters the pool of labile iron to catalytically promote formation of free-radical-mediated stress and oxidative damage to adjacent cells, including neurons. Healthy neurons may also chronically acquire iron from the extracellular space as another principle mechanism for oxidative stress-mediated damage. Pharmacological handling of monocyte migration into the CNS combined with chelators that neutralize the effects of extracellular iron occurring due to the release from dying macrophages as well as intraneuronal chelation may denote good possibilities for reducing the deleterious consequences of iron deposition in the CNS.
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影响因子：
4.2
作者：
CONNOR, JR;MENZIES, SL;MUFSON, EJ
通讯作者：
MUFSON, EJ
影响因子：
3.7
作者：
Biron KE;Dickstein DL;Gopaul R;Jefferies WA
通讯作者：
Jefferies WA
影响因子：
4.8
作者：
Bechmann, I;Goldmann, J;Priller, J
通讯作者：
Priller, J
影响因子：
3.5
作者：
Boserup, Michael W.;Lichota, Jacek;Moos, Torben
通讯作者：
Moos, Torben
影响因子：
4.6
作者：
Biron, Kaan E.;Dickstein, Dara L.;Jefferies, Wilfred A.
通讯作者：
Jefferies, Wilfred A.